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Fish oil supplementation attenuates changes in plasma lipids caused by dexamethasone treatment in rats.

Authors
  • Barbosa, Amanda Marreiro1, 2
  • Francisco, Priscila de Cássia1
  • Motta, Katia1
  • Chagas, Thayz Rodrigues1
  • Dos Santos, Cristiane1
  • Rafacho, Alex1
  • Nunes, Everson Araújo1, 2
  • 1 a Laboratory of Investigation in Chronic Diseases, Department of Physiological Sciences, Center of Biological Sciences, Federal University of Santa Catarina (UFSC), Florianópolis, Brazil.
  • 2 b Multicenter Graduate Program in Physiological Sciences, Graduate Program in Nutrition, Center of Health Sciences, UFSC, Florianópolis, Brazil.
Type
Published Article
Journal
Applied Physiology Nutrition and Metabolism
Publisher
Canadian Science Publishing
Publication Date
April 2016
Volume
41
Issue
4
Pages
382–390
Identifiers
DOI: 10.1139/apnm-2015-0487
PMID: 26939043
Source
Medline
Keywords
License
Unknown

Abstract

Dexamethasone is an anti-inflammatory glucocorticoid that may alter glucose and lipid homeostasis when administered in high doses or for long periods of time. Omega-3 fatty acids, present in fish oil (FO), can be used as potential modulators of intermediary glucose and lipid metabolism. Herein, we evaluate the effects of FO supplementation (1 g·kg(-1) body weight (BW)) on glucose and lipid metabolism in rats treated with dexamethasone (0.5 mg·kg(-1) BW) for 15 days. Adult male Wistar rats were distributed among 4 groups: control (saline, 1 mL·kg(-1) BW and mineral oil, 1 g·kg(-1) BW), DEX (dexamethasone and mineral oil), FO (fish oil and saline), and DFO (fish oil and dexamethasone). Dexamethasone and saline were administered intraperitoneally, and fish oil and mineral oil were administered by gavage. We evaluated functional and molecular parameters of lipid and glycemic profiles at 8 days and at the end of treatment. FO supplementation increased hepatic docosahexaenoic acid (DEX: 5.6% ± 0.7%; DFO: 10.5% ± 0.8%) and eicosapentaenoic acid (DEX: 0.3% ± 0.0%; DFO: 1.3% ± 0.1%) contents and attenuated the increase of plasma triacylglycerol, total cholesterol, and non-high-density lipoprotein cholesterol concentrations in DFO rats compared with DEX rats. These effects seem not to depend on hepatic expression of insulin receptor substrate 1, protein kinase B, peroxisome proliferator-activated receptor γ coactivator 1-α, and peroxisome proliferator-activated receptor γ. There was no effect of supplementation on body weight loss, fasting glycemia, and glucose tolerance in rats treated with dexamethasone. In conclusion, we show that FO supplementation for 15 days attenuates the dyslipidemia induced by dexamethasone treatment.

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